The effect of experimental atherosclerosis, copper deficiency, and magnesium deficiency on elastin metabolism will be studied in the attempt to determine the alterations in elastin that appear related to atherogenesis. Properties of tropoelastin will be studied that are related to elastin calcification. Using appropriate radioisotopes the turnover and relative rates of tropoelastin metabolism will be studied as influenced by diet and experimental treatment. The technique of nutritional copper deficiency will be used to obtain quantities of tropoelastin for physical studies on the protein. The protein will also be used as substrate in assays for proteolytic activities related to elastin digestion and degradation. Assays will be developed to determine elastase activity in aortic tissue using the native substrates (tropoelastin and fibrous elastin). The effect of calcium and cholesterol binding on modification of elastin structure and metabolism will represent a major aspect of the study. The uptake of Ca-45 and P- 32 into aortic tissue and the role of pyrophosphate and pyrophosphatase in the inhibition of calcium deposition in aorta tissue will be included in the investigation with respect to effects of nutritional magnesium deficiency and dietary cholesterol. The effect of those conditions related to the remodeling of aorta tissue (catheptic activity, elastase, elastin turnover) will be assessed in terms of the degree of atherosclerosis and vascular tissue alterations. The atherosclerotic model will be developed using chicks. The assessment of elastin turnover, factors related to aortic calcification, and changes in various proteolytic activities will be measured sequentially as the development of vascular lesions progress.